heart failure in children
Introduction
Introduction to pediatric heart failure The definition of generalized heart failure (heartfailure) is the concept of pathophysiology, that is, heart failure is a cardiac dysfunction, cardiac output can not meet the needs of the body, clinical heart failure is a serious stage of various heart diseases, is a syndrome It consists of 4 parts: cardiac dysfunction, decreased exercise endurance, pulmonary and systemic hyperemia, and late arrhythmia. Cardiac dysfunction is a necessary condition for heart failure. The other three parts are the clinical manifestations of cardiac dysfunction compensation mechanism. . basic knowledge The proportion of illness: 0.001% Susceptible people: children Mode of infection: non-infectious Complications: respiratory failure, heart failure
Cause
Causes of heart failure in children
(1) Causes of the disease
To diagnose heart failure, the cause should be clarified first. Heart failure can occur in the fetal period, and infancy is more common in childhood.
Congenital cardiovascular malformation (35%):
The main cause of heart failure in infancy is congenital cardiovascular malformation, common ventricular septal defect, complete vascular transposition, aortic coarctation, patent ductus arteriosus and endocardial pad defect, heart failure occurs after birth Left ventricular dysplasia syndrome, complete transposition of the most common arteries, myocarditis, severe pneumonia, endocardial fibroelastosis and paroxysmal supraventricular tachycardia are the main causes of heart failure in infancy, in recent years The incidence of Kawasaki disease is increasing, which is one of the causes of heart failure in infants and young children.
Rheumatic fever (20%):
The cause of congestive heart failure in children after 4 years old is mainly rheumatic fever and cardiomyopathy. The main lesions of heart failure caused by rheumatic fever are two: 1 acute myocarditis or carditis.
2 left chronic valvular disease, mainly in children before, myocarditis such as viral myocarditis, diphtheria myocarditis and acute streptococcal infection caused by infectious myocarditis often acute congestive heart failure, severe anemia and vitamin B1 deficiency Other diseases, such as affecting myocardial function, can cause heart failure, Keshan disease is a local cardiomyopathy in China, can occur in childhood, rarely seen before the age of 2, is the main cause of heart failure in epidemic areas, pediatric plateau heart disease It is more common in highland areas with an altitude of 3000m and above. It is preliminarily believed that the increase of vascular resistance caused by the contraction of anterior pulmonary arterioles in the hypoxic capillaries is the cause of this disease. In Qinghai Plateau, the prevalence of children is 0.96%, which is higher than that of adults. High, the prevalence rate of the first to third generations of the displaced population is significantly higher than that of the living population, especially the Han nationality is more sensitive to hypoxia, and the incidence is higher than 2800 m above sea level. The main clinical manifestations are pulmonary hypertension and right ventricular overload. , Tibet and Qinghai Province (1964) 291 clinical reports, high incidence in winter and spring, more common in infants less than 1 year old, early clinical manifestations of crying at night Shortness of breath and periorbital bruising, the tricuspid valve area has a persistent systolic murmur and gradually increases, and the diastolic murmur in the pulmonary valve area is severe, followed by a right heart-based congestive heart failure. X-ray examination showed pulmonary artery bulging, right ventricular enlargement and increased lung texture. Electrocardiogram showed right ventricular hypertrophy or bilateral ventricular hypertrophy. Respiratory tract infection was often the cause of the disease. The main cause of death was heart failure.
In addition, rapid entry into the plateau area, acute plateau pulmonary edema, acute onset, oxygen, sedation, diuretic and intravenous infusion of aminophylline, etc., can be completely restored, other rare causes such as infective endocardium Inflammation, pulmonary heart disease, vitamin B1 deficiency, heart glycogen storage disease and high blood pressure, excessive intravenous fluid or excessive speed can cause acute heart failure, especially in malnourished infants, acute pericardium Inflammation, pericardial effusion and chronic constrictive pericarditis can cause venous return obstruction, venous stasis, insufficient ventricular diastolic filling, decreased heart rate, and diastolic failure.
Other (15%):
1 infection: especially respiratory infections, left-to-right shunt congenital cardiovascular malformations often cause heart failure due to pneumonia; rheumatic fever is the main cause of heart failure caused by rheumatic heart disease, 2 overwork and emotional agitation, 3 anemia 4 arrhythmia: paroxysmal supraventricular tachycardia is common, 5 sodium intake is too much, 6 premature digitalis or digitalis overdose.
(two) pathogenesis
The pathophysiological changes of heart failure are very complicated. Many problems are still unclear. Heart failure is not only a hemodynamic disorder, but also a group of neurohumoral factors involved in the regulation of molecular biology.
1. The main factors regulating heart function
The pump function of the heart is to suck back the blood from the vein and then into the arterial system to maintain the stroke volume to supply the tissue metabolism. The regulation of cardiac output depends on the following factors:
(1) Capacity load: also known as preload, refers to the amount of blood return or end-diastolic volume, usually expressed as diastolic pressure. According to Stalling's law, myocardial contractility is positively correlated with myocardial fiber length within a certain range. When the end-diastolic volume of the ventricle increases, the myocardial fibers are elongated, the myocardial contractility is enhanced, and the cardiac output is increased. However, when the volume exceeds the critical level, the cardiac output is decreased, and the ventricular end-diastolic capacity is related to the diastolic filling time and ventricular compliance. Under certain filling pressure, the filling time is longer, the ventricular end-diastolic volume is increased, the stroke volume is increased, and when the ventricular compliance is decreased, the relationship between diastolic pressure and volume is changed, and the pressure is increased at any capacity, followed by left Increased atrial pressure, pulmonary venous congestion, and pulmonary edema, in addition, ventricular stiffness during diastole, affecting ventricular filling, limiting cardiac output.
(2) Pressure load: also known as post-load, that is, the impedance faced by the ventricle when it begins to contract and ejection. Total peripheral resistance is an important determinant of left ventricular afterload. It can be expressed by blood pressure. When myocardial contractility and preload are constant, after The load decreases and the cardiac output increases; otherwise, it decreases.
(3) Myocardial contractility: refers to the contractile force of the myocardium itself, which is related to the process of myocardial metabolism and excitatory-contraction coupling. It is mainly regulated by the sympathetic nervous system. When the receptor is excited, the myocardial contractility is enhanced and the cardiac output is increased.
(4) Heart rate: related to the electrophysiological characteristics of the cardiac conduction system and cardiac autonomic regulation, cardiac output = heart rate × stroke volume, heart rate changes can affect the stroke volume and cardiac output, increase the heart rate within a certain range Improve cardiac output, when tachycardia, heart rate> 150 times / min, ventricular diastolic filling period is short, filling is insufficient, stroke volume is reduced, cardiac output is reduced, bradycardia, heart rate <40 times / min, diastolic The filling period has reached the limit, and the amount of heart beat can no longer be increased, and thus the cardiac output is reduced.
(5) Coordination of ventricular contraction movement: When the ventricle contracts, the wall motion coordination can maintain the maximum stroke volume, myocardial ischemia, inflammation, can cause contradictory movement of the wall; arrhythmia can make the atrioventricular movement uncoordinated, Both of them can cause a decrease in stroke volume. Among the above factors, the first four items are the most important. If the disorder is adjusted, the heart dysfunction is caused and the cardiac output is reduced.
2. The regulation mechanism of the neuroendocrine system of heart failure
Myocardial injury is the basic cause of heart failure. Ischemia, infection, toxins and mechanical stress can damage the myocardium, resulting in a decrease in the number of normal functioning cardiomyocytes. The cardiac output is reduced, thereby activating the heart, blood vessels and kidneys. The stable regulation mechanism in the series, the early interaction of these adjustment mechanisms in heart failure is beneficial to increase the stroke volume, so that the cardiac output can maintain the body's needs when resting, and then turn into unfavorable factors, promote the development of heart failure, and even the heart function. Clinical signs of decompensation.
(1) Sympathetic nervous system: decreased cardiac output, reflective excitatory sympathetic nerves, a large amount of norepinephrine (NE) and adrenaline released from the sympathetic nerve endings and adrenal medulla to the blood circulation, elevated levels of catecholamines in the blood, so that Impaired myocardial contractility, increased heart rate, peripheral vasoconstriction, partial compensatory hemodynamic abnormalities in early heart failure, but persistently increased sympathetic tone, will bring significant side effects:
1 myocardial metabolism increases, oxygen consumption increases;
2 myocardial receptor density is down-regulated, myocardial contractility is decreased;
3 peripheral vasoconstriction, resulting in excessive load on the heart, increased wall stress and insufficient tissue perfusion;
4 direct myocardial toxicity, causing myocardial necrosis;
5 activation of the renin angiotensin aldosterone system, further aggravating peripheral vasoconstriction and water and sodium retention.
(2) Endocrine system: rapid activation of the circulating endocrine system in the early stage of myocardial injury, including sympathetic and renin angiotensin aldosterone system, so that cardiac function is compensated, clinical signs of heart failure do not appear, but the above internal stability regulation mechanism continues And activates autocrine and paracrine secretion of the heart, blood vessels and other tissues. The former acts on its own cells; the latter acts locally, acting on neighboring cells, and autocrine and paracrine play an important role in the progression of heart failure progression. .
1 Renin angiotensin aldosterone system (RAAS): activation of RAAS is a major neurohumoral regulation process, with decreased renal perfusion and sympathetic excitation during heart failure, stimulation of the release of renin from the glomerulus, activation The main mechanism of RAAS, but the low-sodium diet and diuretics in patients with heart failure are also important factors in the activation of RAAS. The renin in the blood catalyzes the angiotensinogen secreted by the liver to angiotensin I, which passes through the pulmonary vascular bed. The conversion enzyme (ACE) is hydrolyzed to angiotensin II (Ang II). AngII has a stronger contractile vasculature than NE, and stimulates the spheroidal band of the adrenal cortex to increase the secretion of aldosterone (Ald), causing sodium retention and potassium, magnesium. In addition, ACE and kininase II are the same enzyme, which can catalyze the degradation and inactivation of bradykinin, decrease the level of plasma bradykinin, and reduce the synthesis of prostaglandin E, which has diastolic vasolysis, thus aggravating vasoconstriction. Sustained over-activation of RAAS can worsen heart failure. It has been confirmed that AngII can cause myocardial necrosis and promote atherosclerosis in addition to strong contraction of peripheral blood vessels; excessive Ald promotes potassium and magnesium excretion. The threshold of arrhythmia is decreased, and the deposition of myocardial collagen fibers is caused. In addition to the endocrine system, the heart, blood vessels and brain tissues have their own RAAS. When the heart is overloaded, the wall stress increases, and the cardiomyocytes are activated. AngII binds to the cell membrane AngII receptor, and through a series of molecular biology and biochemical processes, the gene expression of cardiomyocytes is abnormal, which promotes the deterioration of heart failure.
2 Atrial natriuretic peptide (ANP): is a secretory of atrial muscle synthesis, with sodium, urinating, dilating blood vessels and inhibiting RAAS. In heart failure, ANP levels in peripheral blood are 2 to 10 times higher than normal controls, prompting ANP The factors of release include:
A. Heart failure causes left and right atrial pressure to rise.
B. The extracellular fluid capacity expands during heart failure, leading to atrial dilatation. Clinical observations show that ANP levels in peripheral blood are positively correlated with the severity of heart failure, the condition is improved, ANP levels are rapidly decreasing, and in the case of heart failure, the activation of natriuretic peptide may be one. A protective neuroendocrine mechanism has an antagonistic effect on excessive RAAS activation and has a beneficial effect on delaying the progression of the disease. Although the heart failure is accompanied by an increase in ANP secretion, its effect is weakened, possibly due to decreased receptor density and decomposition. Hyperthyroidism or renal blood flow is reduced.
3 Growth hormone (GH): In recent years, research on GH is an indispensable factor in heart development and function in adults and in maintaining heart shape and function in adults. GH is secreted by the pituitary gland, and most of its effects are through insulin-like growth factor-1 (IGF- 1) mediated, the latter can be synthesized in the heart, play a paracrine and autocrine role in the myocardium, in addition, IGF-1 produced by other tissues can also act on myocardial tissue, the expression of GH receptor in the myocardium is higher than other Organization, the direct effects of GH on cardiac function are:
A. Promote myocardial tissue growth and regulate cardiac structure.
B. Increase myocardial contractility.
C. Improve the effect of energy conversion to mechanical force.
D. Inhibition of cardiomyocyte apoptosis, the therapeutic effects of GH and IGF-1 in heart failure are still under investigation.
4 Endothelin (ET): vascular endothelium secretes vasoactive substances, regulates vasoconstriction and relaxation of blood vessels, vasoactive substances of endothelium have ET, etc., soothing factors such as nitric oxide (NO) and prostaglandin (PGI2), heart failure Insufficient myocardial oxygen supply, vascular endothelial injury, secretion of vasoactive substances and regulation of vascular dysfunction, mainly manifested by increased secretion of vasoconstrictor, and decreased secretion of vasodilators. Clinical studies have shown that endothelial cells in the heart of patients with heart failure increase The release of ET is increased, and the degree of increase is parallel with the severity of heart failure. ET has a strong vasoconstriction effect, which can contract the resistance vessels and coronary arteries, aggravate the load and myocardial ischemia, and cause pulmonary hypertension and promote vascular smooth muscle, myocardial cells. The role of growth and proliferation.
5 vasopressin (AVP): decreased cardiac output, stimulates the release of AVP from the pituitary gland through cardiovascular baroreceptors. In addition, elevated levels of AngII in the circulation can also promote AVP secretion, and AVP has contractile blood vessels and antidiuretic effects.
6 cytokines: immune dysfunction in patients with heart failure, studies have shown that many cytokines such as tumor necrosis factor- (TNF-), interleukin-2, interleukin-6 and other factors involved in the development of heart failure, clinical observations show that the heart The TNF- level in the blood of patients with aging is related to the severity of heart failure. TNF- also inhibits myocardial contractility and promotes cardiomyocyte apoptosis. In recent years, neuroendocrine research in heart failure is constantly being explored. The aim is to find more effective treatments to control the development of heart failure to prolong the life of patients.
3. Regulation mechanism of ventricular remodeling
In recent years, ventricular remodeling is considered to be a very important part of heart failure, including changes in ventricular mass, ventricular volume, ventricular morphology and structure. It is characterized by a diminished ventricular contractility and a gradual enlargement of the ventricle. The mechanism of ventricular remodeling is not It is clear, but closely related to the changes in molecular biology and biochemistry of cardiomyocytes and the regulation of endocrine, paracrine and autocrine. Studies have shown that when the heart is overloaded, ventricular stress increases, pulling the myocardial cell membrane and activating intracellular AngII, which binds to the cell membrane AngII receptor as an autocrine form, activates protein kinase C through intracellular inositol triphosphate and diacylglycerol pathways, promotes transcription and synthesis of new contractile proteins; acts on the nucleus, and activates the original The transcription and expression of oncogenes further promote the division and proliferation of cardiomyocytes.
The above process makes the surviving cardiac hypertrophy, but the contractile protein gene expression of this hypertrophic myocardium is abnormal, similar to the embryonic phenotype. This embryonic isoform is prone to fatigue, shortens the life span of cardiomyocytes, accelerates myocardial cell failure, and myocardial extracellular matrix. Changes, collagen deposition and fibrosis play an important role in ventricular remodeling. Collagen damage can occur before myocardial necrosis. Studies have shown that activation of AngII and Ald plays an important role in promoting collagen deposition and fibrosis, leading to further expansion of the ventricle. Ventricular remodeling is a poor adaptation process. Hypertrophic cardiomyocytes and collagen fibers are not normal cells, which eventually lead to deterioration of heart failure. Recent studies have shown that attenuated cardiomyocytes undergo programmed cell death and become apoptosis in dilated myocardium. The disease is particularly obvious. It is an important factor leading to the progression of heart failure. Apoptosis and necrosis are different. Apoptosis is not accompanied by inflammatory reaction. Apoptosis is a gene-programmed energy-consuming process. A series of closely related molecular biology and biochemistry The process consists of factors that promote cardiomyocyte apoptosis in the failing heart, including Nitric oxide, reactive oxygen species, cytokines, hypoxia and mechanical stress, cardiomyocyte apoptosis involved in cardiac remodeling during heart failure. Recent animal experiments have confirmed that the heart reserve function of newborn sheep and young sheep is worse than that of adult sheep. Clinical neonates and small babies are also prone to heart failure in older children for the following reasons:
1 The number of sarcomere is small, and the myocardial contractility is weak.
2 Myocardial structure is immature and ventricular compliance is poor.
3 cardiac output is relatively large, the primary child is 300ml / kg, adolescents are 100ml / kg, that is, in the resting state also requires a higher cardiac output to maintain the body's metabolic needs.
4 When the heart rate is quiet, the baby is 120-140 times/min, and the compensatory function generated by increasing the heart rate and cardiac output is limited.
Prevention
Pediatric heart failure prevention
Infection, fatigue and mental agitation in children with heart disease are the main factors in inducing heart failure and should be actively prevented. In some cases, the dose of digitalis should be taken for a long time to prevent heart failure. Actively prevent and treat various organic heart diseases. Prevention and treatment of respiratory tract infections, rheumatism, avoiding overwork, controlling arrhythmia, limiting sodium salt, avoiding the use of drugs that inhibit myocardial contractility, and having prenatal or premature gestational dysfunction should be controlled. 3 Active prevention and treatment of heart function. Symptoms, such as hyperthyroidism, anemia and renal insufficiency.
Complication
Complications of pediatric heart failure Complications, respiratory failure, heart failure
Pulmonary circulation, systemic congestion, peripheral circulatory disorders, cardiogenic shock, obstructive emphysema, ascites and concurrent infections. Obstructive emphysema refers to a pathological state in which the elasticity of the lung tissue at the distal end of the terminal bronchioles is decreased, the volume is enlarged, and the gas content is increased. Severe emphysema can lead to hypoxemia and hypercapnia due to ventilatory and ventilation dysfunction, leading to pulmonary heart disease, and finally respiratory failure and heart failure.
Symptom
Symptoms of pediatric heart failure Common symptoms Diastolic galloping fatigue Arrhythmia hoarseness Paroxysmal nocturnal dyspnea Irritability Unsatisfied pale sputum snoring snoring shortness of breath
Symptoms and signs of heart failure are caused by dysregulation of dysfunction, and due to primary heart disease and age of children, sympathetic excitation, water and sodium retention, pulmonary circulation and systemic venous congestion, and heart failure in elderly children Adults are similar, while newborns and babies are very different. Early neonatal manifestations are often atypical, such as lethargy, apathy, fatigue, refusal to eat or vomiting, weight loss is not obvious, sometimes simply irritability, angina pectoris, these non-specific symptoms are often Neglected, infant heart failure is more acute, rapid development, myocarditis, endocardial fibroelastosis, paroxysmal supraventricular tachycardia, sudden irritability, difficulty breathing, inhalation on the sternum Concave and costal sag, breathing accelerated to 60 times / min, even up to 100 times / min; pale, sweaty, cold limbs, weak pulse, heart rate > 190 beats / min, galloping, lungs wheezing, Liver, congenital heart disease left to right shunt, a little slow onset, feeding difficulties, shortness of breath when sweating, sweating, often interrupted due to difficulty breathing, even refused to eat, weight does not increase, irritability , sweating, like to hug and lie on the shoulders of adults; breathing, dry cough; due to the dilated pulmonary artery or left atrium compression of the recurrent laryngeal nerve, the child crying weak, hoarseness; anterior region of the anterior region, apex beat strong, The tachycardia, the liver is large, the lungs have wheezing; the jugular vein engorgement and edema are not obvious, and there is no edema in the body weight.
Clinical manifestation
The typical clinical manifestations of children with heart failure can be divided into three aspects:
(1) Sympathetic excitation and cardiac dysfunction:
1 tachycardia: infant heart rate > 160 beats / min, school-age children > 100 beats / min, is the early occurrence of compensation phenomenon, in the case of decreased heart rate, tachycardia can increase cardiac output within a certain range To improve tissue hypoxia.
2 irritability: often crying.
3 loss of appetite: anorexia.
4 hyperhidrosis: especially in the head, due to compensatory enhancement of sympathetic excitability.
5 activities are reduced.
6 less urine.
7 heart enlargement and hypertrophy: X-ray can help diagnose, but should be noted for newborns and babies, the hypertrophy of the thymus can be mistaken for increased heart shadow.
8 galloping horses: the emergence of diastolic galloping due to sudden expansion of the ventricle and rapid filling, suggesting that the child has severe cardiac dysfunction.
9 peripheral circulatory disorders: children with pulse weakness, low blood pressure, narrow pulse pressure, may have odd or alternating veins, cold extremities and skin hair, etc., is a sign of acute systemic blood flow reduction.
10 Developmental malnutrition: insufficient caloric intake due to poor long-term tissue perfusion.
(2) the performance of pulmonary circulation congestion: infants with heart failure often have respiratory dysfunction, seen in left heart failure or pulmonary vein obstruction, pulmonary circulation congestion occurs before systemic congestion, right heart failure.
1 shortness of breath: children with pulmonary vein congestion, pulmonary capillary pressure increased, pulmonary interstitial edema; at this time the respiratory rate is accelerated, the baby can be as high as 60 ~ 100 times / min, heart failure is serious, resulting in alveolar and bronchioles edema Difficulty breathing, accompanied by three concave signs.
2 wheezing sound: small airway resistance increased wheezing sound, is a sign of infantile left heart failure, should be distinguished from bronchiolitis, bronchial asthma and bronchial pneumonia, children with bronchioles and mucosal edema, exhalation Obstructed, obstructive emphysema can occur.
3 wet voice: children with alveolar accumulation of a certain amount of fluids appear wet voice, sometimes visible bloody foam sputum, infancy can not hear wet voice.
4 cyanosis: When the alveolar effusion affects the gas exchange, the cyanosis can be seen. If the child has a congenital heart disease with reduced PaO2 (such as transposition of the aorta, ectopic return of the pulmonary vein, etc.), if pulmonary venous congestion occurs, The PaO2 is further lowered, and the cyanosis is aggravated.
5 Dyspnea: Difficulty after exercise and paroxysmal nocturnal dyspnea, is a characteristic of left heart failure in older children. Infants are characterized by difficulty in feeding, prolonged breastfeeding time and wish to hug.
6 cough: bronchial mucosal congestion can cause dry cough, such as cough, or accompanied by fever, you should consider a lung infection.
(3) the performance of systemic venous congestion: children with systemic congestion often occur on the basis of left heart failure or pulmonary hypertension, but can also appear alone, such as pulmonary stenosis, constrictive pericarditis.
1 Liver enlargement: Liver enlargement is the earliest and most common sign of venous congestion. The normal infant's liver can be 2cm below the rib. If it exceeds this limit and the edge is blunt, heart failure should be considered. Progressive increase is more common. Significance, older children can complain of pain or tenderness in the liver area, long-term liver congestion, mild jaundice can occur.
2 jugular vein engorgement: elderly patients with right heart failure and more jugular vein anger; infants due to short neck, subcutaneous fat, not easy to show, the young children's back vein filling is full, is also a common sign of venous congestion.
3 edema: subcutaneous edema in adults and elderly children is an important sign of right heart failure, but in infants due to the volume of the vascular bed is relatively large, so edema is not obvious, generally only mild edema of the eyelids, but daily weight measurement Increase is an objective indicator of fluid retention. Ascites and systemic edema are only seen in older children or children with constrictive pericarditis and restrictive cardiomyopathy.
4 abdominal pain: due to visceral congestion and liver enlargement.
2. Heart function classification
(1) Adults and children: Cardiac function status of heart disease patients can be divided into 4 levels according to medical history, clinical manifestations and labor endurance:
Level 1I: The physical activity of the patient is not restricted.
Level 2II: When the patient is working hard, the patient has symptoms.
Grade 3III: There are obvious symptoms when working lightly, and activities are obviously limited.
Grade 4IV: In the resting state, there are often breathing difficulties or liver enlargement, and the labor is completely lost.
(2) Infants: The above-mentioned cardiac function classification is used for adults and children. It is not suitable for infants. Some authors believe that most of the heart failure of infants is caused by a large left-to-right shunt, which leads to increased blood volume in the pulmonary circulation and is congested. Mainly dysfunction, the classification of cardiac function should accurately describe the feeding history, respiratory rate, respiratory form such as nose fan, three concave and sputum breathing, heart rate, peripheral perfusion, diastolic gallop and liver enlargement The evaluation of baby heart function is graded as follows:
Level 10: No heart failure.
Grade 2I: mild heart failure, the indication is that each breastfeeding amount is <105ml, or breastfeeding time is more than 30min, breathing is difficult, heart rate is >150 beats/min, there may be galloping, and the liver is enlarged 2cm under the rib.
Grade 3II: moderate heart failure, indicated as <90ml per lactation, or more than 40min during breastfeeding, >60 breaths/min, abnormal breathing pattern, heart rate >160 beats/min, 2 lobes under the liver 3cm, there are galloping horses, grade 4III: severe heart failure, indication is <75ml for each breastfeeding, or more than 40min for breastfeeding, breathing >60 beats/min, abnormal breathing pattern, heart rate >170 beats/min, Running horses, more than 3cm under the liver ribs, and poor perfusion of the peripheral, and according to the clinical manifestations of heart failure, the infant heart failure grading score table (Table 2), for infant heart failure classification.
3. Heart function monitoring
Cardiac function should be detected in children with severe heart failure, including vital signs and interventional hemodynamic monitoring. The parameters should be observed continuously and recorded in detail so that the treatment measures can be modified in time.
(1) Heart rate and rhythm: ECG shows continuous monitoring of heart rate and arrhythmia.
(2) Respiratory frequency: monitor the respiratory condition if necessary, the heart rate and respiratory rate of normal children of different ages.
(3) Blood pressure: reflecting left ventricular afterload, heart failure, cardiac output decreased, blood pressure decreased, tissue perfusion was poor, blood pressure was monitored by sphygmomanometer, normal blood pressure values of children of different ages are shown in Table 4, sympathetic in children with cardiac insufficiency Nerve compensatory enhancement, peripheral vasoconstriction, indirect measurement of blood pressure with cuff can not directly reflect arterial pressure, radial artery cannula directly monitor blood pressure, and the average arterial pressure should be recorded, should be maintained at 7.8 ~ 10.4kPa (60 ~ 80mmHg).
(4) body temperature: the anus temperature should be detected, because the peripheral blood vessels of children with severe heart failure contract, the temperature under the armpit is not accurate, the anus temperature 38.5 °C suggests infection.
(5) Arterial blood oxygen: Continuous monitoring of arterial oxygen saturation using a pulse oximeter to detect hypoxemia early and treat it promptly.
(6) central venous pressure: the catheter is inserted into the vena cava near the right atrium to measure the pressure, the central venous pressure is directly related to the right atrial pressure; if the right ventricular physiology and anatomy are normal, it can reflect the right ventricular end-diastolic pressure, clinical The central venous pressure is usually used as an indicator of the right ventricular preload, suggesting a return to the heart and right heart function. The normal value is 0.59 to 1.18 kPa (6 to 12 cm H2O). If it exceeds 1.18 kPa (12 cm H2O), the blood volume is increased. Excessive or infusion volume, infusion rate is too fast; below 0.59kPa (6cmH2O) suggests insufficient blood volume, therefore, central venous pressure can be used as a guide to guide infusion therapy, right ventricular end-diastolic capacity can better reflect the preload, In addition to a certain relationship with end-diastolic pressure, ventricular compliance is also one of the determining factors. When ventricular compliance declines, the end-diastolic volume decreases and the pressure rises.
(7) Pulmonary capillary wedge pressure: measured by floating catheter, the cannula enters the pulmonary artery through the right ventricle, to the end, the balloon at the front end of the catheter is inflated, the pulmonary capillary wedge pressure can be measured, which can indirectly reflect the pulmonary venous pressure, left atrium Pressure and left ventricular end-diastolic pressure, used to evaluate left ventricular preload and left ventricular function, normal value of 1.04 ~ 1.56kPa (8 ~ 12mmHg), such as rose to 2.6kPa (20mmHg) or more, suggesting pulmonary congestion, pulmonary edema or Left heart failure, detection of pulmonary capillary wedge pressure, for guiding expansion, prevention of pulmonary edema, the use of vasodilators and diuretics have reference significance, left ventricular end-diastolic pressure and capacity, but affected by ventricular compliance.
(8) Cardiac output: Cardiac output (Cadiac Output, CO) was measured by thermodilution method, and cardiac index was calculated according to body surface area. Normal pediatric heart index (Cadiac Index, CI) was 3.5-5.5 L/(min·m2 ), in the absence of testing equipment, should closely observe the child's state of mind, blood pressure, heart rate, pulse, breathing, peripheral circulation, liver size, lungs, voice and urine volume, and record every half hour to understand the dynamics Change and treatment response, and develop appropriate treatment measures.
Examine
Pediatric heart failure examination
1. Blood gas and pH
Different hemodynamic changes in children may have corresponding changes in blood gas and pH, volume overload, severe pulmonary vein congestion, due to right-to-left shunt in the lungs and ventilatory-perfusion dysfunction, causing a slight decrease in PaO2, severe cases Alveolar edema, respiratory acidosis; milder disease, only pulmonary interstitial edema, respiratory alkalosis occurs when compensated breathing increases, systemic blood volume is severely reduced, tissue perfusion is poor, acidic metabolites are especially Lactic acid accumulation, leading to metabolic acidosis, arterial blood oxygen tension is severely reduced, such as pulmonary blood flow obstruction, aortic transposition malformation, etc., anaerobic metabolism increases, although the volume of blood circulation is quite large, but the release of oxygen to the tissue is insufficient, can also lead to Metabolic acidosis.
2. Serum electrolyte
Infant heart failure often has hyponatremia, blood sodium is lower than 125mmol / L, reflecting water retention, hypochloremia is seen in the use of diuretics, blood potassium levels can be increased in acidosis, with powerful diuretics can cause Hypokalemia.
3. Blood routine
Severe anemia can lead to heart failure.
4. Urine routine
There may be mild proteinuria and microscopic hematuria.
5. Blood sugar and blood calcium
Newborn patients should measure blood sugar, blood calcium, hypoglycemia or hypocalcemia can cause heart failure.
6. Myocardial enzyme
In patients with myocarditis and myocardial ischemia, creatine phosphokinase (CPK) and isoenzyme (CK-MB) can be elevated.
7. Renal function test
8. X-ray chest
It is very important to evaluate the size of the heart and the condition of the lungs. According to the room, the size of the room, the increase or decrease of pulmonary blood, it can help to make the cause of the diagnosis, and can show pulmonary congestion, pulmonary edema, pleural effusion and enlargement of the bronchus due to pulmonary artery and atrial enlargement. The left lower lung atelectasis, or secondary pneumonia, the normal thymus heart shadow of the baby can be misdiagnosed as enlarged heart and should be noted.
9. ECG
It has diagnostic and guiding therapeutic significance for heart failure caused by arrhythmia and myocardial ischemia.
10. Echocardiography
Cardiac ultrasound technology is used to observe the size of the heart, intracardiac structure, large blood vessel position, blood flow direction and speed, pericardial effusion and cardiac function measurement. It has the advantages of non-invasive, convenient and reproducible, and can be carried out at the bedside for the cause. Cardiac function estimation is important before and after diagnosis and treatment. Heart function is usually measured by two-dimensional echocardiography. Left ventricular systolic function indicators are:
(1) Ejection Fraction (EF): the ratio of the amount of bloodshot bleeding to the end-diastolic volume of the heart at each contraction. The formula is: ejection fraction = (end ventricular end-diastolic volume - ventricular end-systolic volume) / ventricular end-diastolic volume = stroke volume / ventricular end-diastolic volume It reflects the function of the ventricular pump, the stronger the ventricular contractile force, the greater the heart volume, the smaller the residual blood volume in the end-diastolic period, that is, the ejection fraction is increased, the normal value is 0.59 ~ 0.75 (0.67 ± 0.08), such as less than 0.5 to indicate cardiac insufficiency.
(2) Shortening Fraction SF: The ratio of the shortened inner diameter to the end diastolic diameter during ventricular contraction, calculated as: shortened fraction = (end ventricular end diastolic diameter - end systolic end diameter) / ventricular end diastolic diameter Reflecting the ability of myocardial fiber to shorten the systolic phase, the strength of myocardial contraction, the normal value is 0.35±0.03, less than 0.3 indicates cardiac insufficiency, diastolic function measurement using Doppler echocardiography, detection of mitral and tricuspid valves The blood flow spectrum can clearly show the diastolic filling of the ventricle, the E peak is the fast filling blood flow velocity, and the A peak is the atrial systolic blood flow velocity. Through the ventricle main, the passive filling spectrum E and the atrial filling spectrum A, other filling blood can be measured. Flow velocity, velocity-time integral and mutual relationship, etc., E-wave of diastolic heart failure spectrum is reduced, and spectrum A wave can be compensated for increase, then E/A<1, normal E/A>1, such as EF, SF Normal, E/A<1 is diastolic dysfunction. For children with heart failure, ejection fraction <50%, Doppler echocardiography ventricular filling spectrum E/A<1, can initially make diastolic heart Judgment of decline.
11. Cardiac mechanical diagram, cardiac catheterization and judgment of cardiac function test
Some scholars have determined that left ventricular diastolic function is well correlated by cardiac mechanical imaging and cardiac catheter traumatic examination. A/EO, a/CO ratio and left ventricular end-diastolic pressure (LVEOP), compliance with end-diastolic volume in ACG (dV/dpV), left ventricular is closely related to LV (V/pV) and other left ventricular diastolic compliance indicators, and is not affected by heart rate and age. It is a stable index for assessing left ventricular diastolic function, such as its ratio. Increase, suggesting a decrease in diastolic function and compliance in the chamber, and determining hemodynamic measurements of cardiac function:
(1) central venous pressure measurement: can be measured from the venous cannula to the right atrium or the superior and inferior vena cava near the cardiac vein, the normal value is 0.588 ~ 0.981kPa (6 ~ 10cmH2O), when the central venous pressure <0.49kPa ( 5cmH2O), suggesting that the effective blood volume is insufficient, >0.981~1.18kPa (10~12cmH2O), suggesting that the heart is insufficiency or too much fluid, too fast.
(2) Pulmonary capillary wedge pressure: It is an important indicator of hemodynamics. Percutaneous puncture, using a floating tube (Swan-Ganz) balloon catheter with a balloon at the top, after being delivered to the right atrium, the balloon is filled with carbon dioxide. Or filter the air to inflate the balloon, so that the balloon at the tip of the catheter floats in the blood, is pushed forward by the blood flow, floats to the pulmonary artery and is embedded in the terminal branch of the pulmonary artery, and is measured. In the absence of pulmonary vascular disease, the lung is embedded. Consistent with pulmonary venous pressure, and because there is no valve between pulmonary vein and left atrium, pulmonary static pressure reflects left atrial pressure. If there is no mitral stenosis, left atrial pressure reflects left ventricular end-diastolic pressure, mainly reflecting cardiac preload, such as pressure. Elevation suggests the presence of left heart failure, normal 0.8 ~ 1.6kPa (6 ~ 12mmHg), such as PWP 2.4 ~ 2.67kPa (18 ~ 20mmHg) means pulmonary congestion, 2.8 ~ 3.33kPa (21 ~ 25mmHg) is light, medium Degree of pulmonary congestion, 3.47 ~ 4.00kPa (26 ~ 30mmHg) for severe pulmonary congestion, there may be pulmonary edema, such as greater than 4.00kPa (30mmHg) pulmonary edema.
(3) Direct measurement of arterial pressure: In heart failure, due to the sharp drop in cardiac output, the arterial pressure is lower than the necessary tissue perfusion pressure, so the tissue perfusion volume is reduced, so arterial pressure is an important indicator of cardiac pump function and tissue perfusion status. However, when the blood output is decreased, the sympathetic nerves are compensatory and the peripheral arteries are contracted. Therefore, when the blood pressure is measured by the cuff blood pressure meter, the intra-arterial pressure cannot be reflected. Therefore, it is necessary to directly measure with the radial artery puncture or intubation. Correctly reflect left ventricular afterload.
(4) cardiac output: cardiac output refers to cardiac output per minute, normal value 5 ~ 6L / min, heart failure, cardiac output decreased.
(5) Heart index: the normal value of cardiac output per square meter of surface area is 2.6 to 4.0 L/min per square meter, and is reduced in heart failure.
(6) ejection fraction: left ventricular ejection fraction is a sensitive indicator of reactive myocardial pump function, ejection fraction (EF) = (end-diastolic volume - end-systolic volume) / end-diastolic volume.
Diagnosis
Diagnosis and diagnosis of pediatric heart failure
diagnosis
In 1985, the National Diagnostic Standard for Pediatric Heart Failure was discussed and developed.
1. Have the following 4 items to consider heart failure:
(1) shortness of breath: infants > 60 beats / min; infants > 50 beats / min; children > 40 beats / min.
(2) tachycardia: infants > 160 beats / min; infants > 140 beats / min; children > 120 beats / min.
(3) Heart enlargement: physical examination, X-ray or echocardiographic findings.
(4) irritability, difficulty feeding, weight gain, oliguria, edema, sweating, bruising, coughing, paroxysmal dyspnea (more than 2 items).
2. Diagnosis conditions: With the above 4 items, plus one or more of the following 2 items plus the following 2 items, you can diagnose heart failure:
(1) Liver enlargement: infants and young children under the ribs 3cm; children > 1cm; progressive liver enlargement or accompanied by tenderness is more meaningful.
(2) pulmonary edema.
(3) Running horses.
Differential diagnosis
;;X
